ইঙ্গিত
ফার্মাকোলজি
An acute attack of gout apparently occurs as a result of an inflammatory reaction to crystals of monosodium urate that are deposited in the joint tissue from hyperuric body fluids; the reaction is aggravated as more urate crystals accumulate. Leukocytes migrate to the sites where urate crystals have been deposited and try to engulf the crystals by phagocytosis. As a result lactic acid and proinflammatory enzymes are released which cause inflammation with severe pain, redness, and swelling of the affected joint. Lactic acid favors a local decrease in pH that enhances uric acid deposition. Colchicine inhibits the phagocytosis of uric acid by leukocytes & also diminishes the lactic acid production directly. Thus interrupts the cycle of urate crystal deposition and inflammatory response that sustains the acute attack of gout. Colchicine is absorbed when given orally, reaching a mean Cmax of 2.5 ng/mL (range 1.1 to 4.4 ng/mL) in 1 to 2 hours after a single dose administered under fasting conditions. The mean apparent volume of distribution is approximately 5 to 8 L/kg. Colchicine binding to serum protein is low (39 ± 5%), primarily to albumin regardless of concentration. CYP3A4 is involved in the metabolism of Colchicine to 2-O-demethylcolchicine and 3-O-demethylcolchicine. Plasma levels of these metabolites are minimal (less than 5% of parent drug). Following multiple oral doses (0.6 mg twice daily), the mean elimination half-life is 26.6 to 31.2 hours.
Pregnancy & Breastfeeding
Pregnancy Category C. There have been no adequate, well-controlled studies of colchicine in pregnant women. Colchicine passes into breast milk, so nursing mothers should use it only with caution.
⚠️ Talk to your doctor before taking any medicine during pregnancy or while breastfeeding.
ডোজ নির্দেশিকা
⚠️ শুধুমাত্র সরকারি উৎস থেকে নির্দেশিকা পরিসীমা। ব্যক্তিগতকৃত ডোজের জন্য আপনার ডাক্তারের পরামর্শ নিন।
পার্শ্বপ্রতিক্রিয়া ও পারস্পরিক ক্রিয়া
পার্শ্বপ্রতিক্রিয়া
No side-effect data recorded yet.